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eEF-2 Phosphorylation Down-Regulates P-Glycoprotein Over-Expression in Rat Brain Microvessel Endothelial Cells.

Authors: Tang, XH  Wu, XY  Xu, L  Fang, YX  Wang, P  Zhu, GX  Hong, Z 
Citation: Tang XH, etal., PLoS One. 2015 May 11;10(5):e0125389. doi: 10.1371/journal.pone.0125389. eCollection 2015.
Pubmed: (View Article at PubMed) PMID:25962137
DOI: Full-text: DOI:10.1371/journal.pone.0125389

OBJECTIVE: We investigated whether glutamate, NMDA receptors, and eukaryote elongation factor-2 kinase (eEF-2K)/eEF-2 regulate P-glycoprotein expression, and the effects of the eEF-2K inhibitor NH125 on the expression of P-glycoprotein in rat brain microvessel endothelial cells (RBMECs). METHODS: Cortex was obtained from newborn Wistar rat brains. After surface vessels and meninges were removed, the pellet containing microvessels was resuspended and incubated at 37 degrees C in culture medium. Cell viability was assessed by the MTT assay. RBMECs were identified by immunohistochemistry with anti-vWF. P-glycoprotein, phospho-eEF-2, and eEF-2 expression were determined by western blot analysis. Mdr1a gene expression was analyzed by RT-PCR. RESULTS: Mdr1a mRNA, P-glycoprotein and phospho-eEF-2 expression increased in L-glutamate stimulated RBMECs. P-glycoprotein and phospho-eEF-2 expression were down-regulated after NH125 treatment in L-glutamate stimulated RBMECs. CONCLUSIONS: eEF-2K/eEF-2 should have played an important role in the regulation of P-glycoprotein expression in RBMECs. eEF-2K inhibitor NH125 could serve as an efficacious anti-multidrug resistant agent.

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CRRD Object Information
CRRD ID: 11041133
Created: 2016-03-22
Species: All species
Last Modified: 2016-03-22
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.